We hypothesised that polymorphisms of glucocorticoid receptor gene, determining augmented or suppressed sensitivity to glucocorticoids, may have pathogenic significance in the development of SLE and RA, may alter the clinical pattern of the disease. We have found that the prevalence of BclI polymorphism was lower in the SLE group as compared to healthy controls. These findings are in concordance with the fact that BclI polymorphism increases glucocorticoid sensitivity and may have a preventive role in the development of SLE. Presently, our findings show that the more frequent appearance of the minor allele of BclI polymorphism is associated with a lower risk of developing RA by increasing GC sensitivity. In conrast to previous studies, we did not find associations between other investigated GR polymorphisms (N363S, 9β) and the susceptibility to RA. One interesting association was found, however, between carrier status of BclI and neuro-psychiatric symptoms.
These symptoms developed more frequently in the BclI positive SLE group and, in addition, these symptoms were less prevalent in the A3669G carriers The BclI polymorphism increases while the A3669G polymorphism decreases the sensitivity of glucocorticoid receptors and may have influence on the development of psychiatric syndromes. The age at the onset of disease of RA patients without anti-TNFα was significantly higher compared to the patients with anti-TNFα treatment. However, the age of 9ß carrier RA patients was higher but not significantly, than controls, which is controversary knowing its effect causing relative GC resistance. Otherwise, carrying the 9ß SNP may result in the need of anti-TNFα treatment, which may contribute to the significantly lower anti-CCP levels in these patients compared to those not treated with anti-TNFα. Homozygous BclI patients in the RA population and also in the subgroup of patients not treated with anti-TNFα showed a significantly higher aDNA level compared to heterozygous carriers. Homozygous BclI patients treated with anti-TNFα showed only tendency. There was no correlation between the aDNA and aCCP levels in the two (anti-TNFα treated and not-treated) populations, either. According to the GC sensitizing effect of BclI results indicated lower tender joint count in homozygous carriers, altough this association did not reach satistical significance. However, this tendency was consequent regardless of anti-TNFα therapy.
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